Journal of Bone and Mineral Research

Okuda, Ayako; Kanehisa, Junya; Heersche, J. N. M.

doi:10.1002/jbmr.5650051381

Cited by 38 publications

(24 citation statements)

References 16 publications

(6 reference statements)

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“…19 Fluoride can inhibit the function of isolated osteoclasts at 0.5 to 1.0 mmol·L −1 in vitro . 20 Fluoridated drinking water markedly inhibited the bone resorption induced by hydrocortisone 21 and showed a lower histologic incidence of alveolar bone resorption after the injection of parathormone. 22 …”

Section: Discussionmentioning

confidence: 91%

Micromolar sodium fluoride mediates anti-osteoclastogenesis in Porphyromonas gingivalis-induced alveolar bone loss

et al. 2015

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Osteoclasts are bone-specific multinucleated cells generated by the differentiation of monocyte/macrophage lineage precursors. Regulation of osteoclast differentiation is considered an effective therapeutic approach to the treatment of bone-lytic diseases. Periodontitis is an inflammatory disease characterized by extensive bone resorption. In this study, we investigated the effects of sodium fluoride (NaF) on osteoclastogenesis induced by Porphyromonas gingivalis, an important colonizer of the oral cavity that has been implicated in periodontitis. NaF strongly inhibited the P. gingivalis-induced alveolar bone loss. That effect was accompanied by decreased levels of cathepsin K, interleukin (IL)-1β, matrix metalloproteinase 9 (MMP9), and tartrate-resistant acid phosphatase, which were up-regulated during P. gingivalis-induced osteoclastogenesis. Consistent with the in vivo anti-osteoclastogenic effect, NaF inhibited osteoclast formation caused by the differentiation factor RANKL (receptor activator of nuclear factor κB ligand) and macrophage colony-stimulating factor (M-CSF). The RANKL-stimulated induction of the transcription factor nuclear factor of activated T cells (NFAT) c1 was also abrogated by NaF. Taken together, our data demonstrate that NaF inhibits RANKL-induced osteoclastogenesis by reducing the induction of NFATc1, ultimately leading to the suppressed expression of cathepsin K and MMP9. The in vivo effect of NaF on the inhibition of P. gingivalis-induced osteoclastogenesis strengthens the potential usefulness of NaF for treating periodontal diseases.

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Section: Discussionmentioning

confidence: 91%

Micromolar sodium fluoride mediates anti-osteoclastogenesis in Porphyromonas gingivalis-induced alveolar bone loss

et al. 2015

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“…4 It has been shown that fluoride reduced the number of the osteoclasts in bone. 24 Additionally, it has been demonstrated that fluoride decreases the number of resorption lacunae made by individual clast cells, 25 the resorbed area per clastic cells, 16,19,25 and the depth of the clastic cell demineralization pit. 16,19,26 In the present study, high fluoride groups exhibited a decreased amount of root resorption after the application of light and heavy forces for 4 weeks.…”

Section: Discussionmentioning

confidence: 99%

Effect of fluoride on root resorption following heavy and light orthodontic force application for 4 weeks and 12 weeks of retention

Karadeniz

Gonzales

Türk

et al. 2012

The Angle Orthodontist

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Objective: To evaluate the null hypothesis that fluoride intake via drinking water has no effect on orthodontic root resorption in humans after orthodontic force application for 4 weeks and 12 weeks of retention. Materials and Methods: Forty-eight patients who required maxillary premolar extractions as part of their orthodontic treatment were selected from two cities in Turkey. These cities had a high and low fluoride concentration in public water of $2 pm and #0.05 pm, respectively. The patients were randomly separated into four groups of 12 each: group 1HH, high fluoride ($2 ppm) and heavy force (225 g); group 2LH, low fluoride (#0.05 ppm) and heavy force; group 3HL, high fluoride and light force (25 g); and group 4LL, low fluoride and light force. Light or heavy buccal tipping force was applied on the upper first premolars for 28 days. At day 28, the left premolars were extracted (positive control side); the right premolars (experimental side) were extracted after 12 weeks of retention. The samples were analyzed with microcomputed tomography. Results: On the positive control side, under heavy force application, the high fluoride groups exhibited less root resorption (P 5 .015). On the experimental side, it was found that fluoride reduced the total volume of root resorption craters; however, this effect was not statistically significant (P 5 .237). Moreover, the results revealed that under heavy force application experimental teeth exhibited more root resorption than positive control groups. Conclusion: The null hypothesis could not be rejected. High fluoride intake from public water did not have a beneficial effect on the severity of root resorption after a 4-week orthodontic force application and 12 weeks of passive retention. (Angle Orthod. 2013;83:418-424.)

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“…As these findings are similar to the clinical syndrome of skeletal fluorosis in humans, a pathogenic mechanism has been suggested whereby chronic daily consumption of trifluorinated voriconazole molecules leads to excess plasma fluoride, which then promotes the development of periostitis by enhancing the activity of osteoblasts (11,13,17). Although this is consistent with the known clinical and cellular effects of fluoride (19,20,31,32,40), this hypothesis has not been directly evaluated for voriconazole-associated periostitis. Therefore, the goal of this study was to evaluate this hypothesis by assessing the effects of voriconazole exposure on osteoblastic activity in vitro.…”

Section: Discussionmentioning

confidence: 98%

“…Given that bones sequester fluoride over the human life span, it is possible that voriconazole stimulates fluoride release from bone. While fluoride has been demonstrated to inhibit osteoclastic activity in proportion to its concentration (40,45,46), to our knowledge no studies have examined the effects of voriconazole on osteoclasts.…”

Section: Discussionmentioning

confidence: 99%

Voriconazole Enhances the Osteogenic Activity of Human Osteoblasts In Vitro through a Fluoride-Independent Mechanism

Allen

Sánchez

Niece

et al. 2015

Antimicrob Agents Chemother

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b Periostitis, which is characterized by bony pain and diffuse periosteal ossification, has been increasingly reported with prolonged clinical use of voriconazole. While resolution of clinical symptoms following discontinuation of therapy suggests a causative role for voriconazole, the biological mechanisms contributing to voriconazole-induced periostitis are unknown. To elucidate potential mechanisms, we exposed human osteoblasts in vitro to voriconazole or fluconazole at 15 or 200 g/ml (reflecting systemic or local administration, respectively), under nonosteogenic or osteogenic conditions, for 1, 3, or 7 days and evaluated the effects on cell proliferation (reflected by total cellular DNA) and osteogenic differentiation (reflected by alkaline phosphatase activity, calcium accumulation, and expression of genes involved in osteogenic differentiation). Release of free fluoride, vascular endothelial growth factor (VEGF), and platelet-derived growth factor (PDGF) was also measured in cell supernatants of osteoblasts exposed to triazoles, with an ion-selective electrode (for free fluoride) and enzyme-linked immunosorbent assays (ELISAs) (for VEGF and PDGF). Voriconazole but not fluconazole significantly enhanced the proliferation and differentiation of osteoblasts. In contrast to clinical observations, no increases in free fluoride levels were detected following exposure to either voriconazole or fluconazole; however, significant increases in the expression of VEGF and PDGF by osteoblasts were observed following exposure to voriconazole. Our results demonstrate that voriconazole can induce osteoblast proliferation and enhance osteogenic activity in vitro. Importantly, and in contrast to the previously proposed mechanism of fluoride-stimulated osteogenesis, our findings suggest that voriconazole-induced periostitis may also occur through fluoride-independent mechanisms that enhance the expression of cytokines that can augment osteoblastic activity. Invasive fungal infections (IFIs) rarely occur in immunocompetent individuals but are potentially devastating in certain patient populations, including patients undergoing intensive chemotherapy or receiving autologous or allogeneic hematopoietic stem cell transplants for the treatment of hematological malignancies (1, 2). In recent years, there have been reports of cutaneous IFIs among immunocompetent individuals, with traumatic injuries, including motor vehicle accidents, natural disasters, and combat-related trauma, being cited as significant risk factors for infection with environmental molds, of which Aspergillus spp. are among the most commonly isolated (3-5). The recommended therapy for treatment of cutaneous IFIs involves extensive surgical debridement combined with empirical systemic antifungal therapy, for which fluorinated triazoles, including voriconazole, are important options for susceptible fungi. As the incidence rates of IFIs have been reported to be as high as 12% among immunocompromised patients (6) and up to 3.5% among U.S. military personnel admitted ...

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Journal of Bone and Mineral Research

Cited by 38 publications

References 16 publications

Micromolar sodium fluoride mediates anti-osteoclastogenesis in Porphyromonas gingivalis-induced alveolar bone loss

Micromolar sodium fluoride mediates anti-osteoclastogenesis in Porphyromonas gingivalis-induced alveolar bone loss

Effect of fluoride on root resorption following heavy and light orthodontic force application for 4 weeks and 12 weeks of retention

Voriconazole Enhances the Osteogenic Activity of Human Osteoblasts In Vitro through a Fluoride-Independent Mechanism

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